Epigenomics of cardiac myocytes in health and disease
We are seeking a talented bioinformatician to apply their expertise to investigate epigenetic mechanisms controlling cardiac myocyte phenotype and fate choices in postnatal development, disease and ageing. This project will leverage recent data generated in the laboratory and build on our recently published findings (Thienpont, Aronsen, Robinson et al., JCI 2017) contributing to the development of new strategies to target cardiovascular disease. Building on our recently published findings (Thienpont, Aronsen, Robinson et al., JCI 2017), this project aims to dissect the contribution of the epigenome to determining and maintaining the post-mitotic state of the adult cardiac myocyte and how it can be manipulated to ameliorate disease. Given that the absence of proliferation is the Achilles' heel of the adult myocyte, underlying the inadequate proliferation required to repair the damaged heart, identifying how cardiac myocyte fate can be reprogrammed is an exciting and clinically relevant area of research. Moreover, the absence of proliferation in the adult heart provides an ideal substrate to examine epigenetic mechanisms independent of cell cycle.
This project will probe the role of the epigenome in postnatal development of the adult cardiac myocyte and how degradation of the epigenetic landscape contributes to cardiac remodelling in disease and ageing. In this regard, the contribution of cellular heterogeneity to cardiac phenotype will also be investigated by single cell approaches. Through these analysis, nodal regulators and networks will be identified and their contribution to disease/cardiac myocyte phenotype tested in in vivo models and in patient samples. This research will also contribute to identification of strategies (key targets) to manipulate the epigenome to reprogram cardiac myocyte phenotype to the healthy adult state.
Genomic/epigenomic analysis is performed on cardiac myocytes isolated from genetically modified mice (cardiac specific knockout and transgenics, adeno-associated virus transduced), mouse models of disease (aortic banding, myocardial infarction), human tissue and iPS-derived cardiac myocytes. We analyse transcriptomes and epigenomes, including methylomes of cell populations and single cells (next generation sequencing - ChIP-Seq/RNA-Seq/BS-Seq/singlecell RNA-Seq). As evidenced by our publications, we collaborate extensively within KU Leuven and outside to advance our research.
Your role: If you are a talented scientist,with a special interest in working as part of a team to identify epigenetic mechanisms controlling cell fate transitions and disease processes in a biomedical context, please apply. You will work closely with bench scientists in the laboratory and in addition to your own project, you will have opportunities to collaborate on other related projects. It is also important that you have the ambition to dig deeper than the obvious and perform important research that is relevant to human disease mechanisms.
Thienpont, B., J.M. Aronsen, E.L. Robinson, H.Okkenhaug, E. Loche, A. Ferrini, P. Brien, K. Alkass, A. Tomasso, A. Agrawal,O. Bergmann, I. Sjaastad, W. Reik, and H.L. Roderick. ... For more information see https://icts.kuleuven.be/apps/jobsite/vacatures/54343852
This job comes from a partnership with Science Magazine and